ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
Activation of peroxisome proliferator-activated receptor-γ by rosiglitazone improves lipid homeostasis at the adipose tissue-liver axis in ethanol-fed mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 83 citations in OpenAlex.
- Systemic Consequences of Chronic Ethanol Intake: From Microbiome Shifts to Metabolic Impairment.Comprehensive physiology · 2026Article
- Article
- Chronic binge alcohol dysregulates omental adipose tissue extracellular matrix in simian immunodeficiency virus-infected macaques.Alcohol, clinical & experimental research · 2025Article
- ASPP2 deficiency attenuates lipid accumulation through the PPARγ pathway in alcoholic liver injury.Cell biology and toxicology · 2024Article
- Peroxisome proliferator-activated receptor agonists: A new hope towards the management of alcoholic liver disease.World journal of gastroenterology · 2024Article
- Reversal of hepatic accumulation of nordeoxycholic acid underlines the beneficial effects of cholestyramine on alcohol-associated liver disease in mice.Hepatology communications · 2024Article
- Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue.Biochemistry and biophysics reports · 2024Article
- Aldo-keto reductase family 1 member A1 (AKR1A1) exerts a protective function in alcohol-associated liver disease by reducing 4-HNE accumulation and p53 activation.Cell & bioscience · 2024Article
- Class III Alcohol Dehydrogenase Plays a Key Role in the Onset of Alcohol-Related/-Associated Liver Disease as an S-Nitrosoglutathione Reductase in Mice.International journal of molecular sciences · 2023Article
- Alcohol, White Adipose Tissue, and Brown Adipose Tissue: Mechanistic Links to Lipogenesis and Lipolysis.Nutrients · 2023Review
- In vitro, in vivo, and in silico analysis of synbiotics as preventive interventions for lipid metabolism in ethanol-induced adipose tissue injury.Lipids in health and disease · 2023Article
- 4-PBA inhibits hypoxia-induced lipolysis in rat adipose tissue and lipid accumulation in the liver through regulating ER stress.Food science & nutrition · 2023Article
- Remodeling of dermal adipose tissue alleviates cutaneous toxicity induced by anti-EGFR therapy.eLife · 2022Article
- Gut Microbiota: Target for Modulation of Gut-Liver-Adipose Tissue Axis in Ethanol-Induced Liver Disease.Mediators of inflammation · 2022Review
- A review of the role of ethanol-induced adipose tissue dysfunction in alcohol-associated liver disease.Alcoholism, clinical and experimental research · 2021Review
- Therapeutic potential of PPARγ natural agonists in liver diseases.Journal of cellular and molecular medicine · 2020Review
- Role of Mechanistic Target of Rapamycin and Autophagy in Alcohol-Induced Adipose Atrophy and Liver Injury.The American journal of pathology · 2020Article
- Lipid droplet dynamics in alcoholic fatty liver disease.Liver research (Beijing, China) · 2019Article
- Alcohol-induced adipose tissue macrophage phenotypic switching is independent of myeloid Toll-like receptor 4 expression.American journal of physiology. Cell physiology · 2019Article
- Inhibition of Ghrelin Activity by Receptor Antagonist [d-Lys-3] GHRP-6 Attenuates Alcohol-Induced Hepatic Steatosis by Regulating Hepatic Lipid Metabolism.Biomolecules · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The development of alcohol-induced fatty liver is associated with a reduction of white adipose tissue (WAT). Peroxisome proliferator-activated receptor (PPAR)-γ prominently distributes in the WAT and plays a crucial role in maintaining adiposity. The present study investigated the effects of PPAR-γ activation by rosiglitazone on lipid homeostasis at the adipose tissue-liver axis. Adult C57BL/6 male mice were pair fed liquid diet containing ethanol or isocaloric maltose dextrin for 8 wk with or without rosiglitazone supplementation to ethanol-fed mice for the last 3 wk. Ethanol exposure downregulated adipose PPAR-γ gene and reduced the WAT mass in association with induction of inflammation, which was attenuated by rosiglitazone. Ethanol exposure stimulated lipolysis but reduced fatty acid uptake capacity in association with dysregulation of lipid metabolism genes. Rosiglitazone normalized adipose gene expression and corrected ethanol-induced lipid dyshomeostasis. Ethanol exposure induced steatosis and upregulated inflammatory genes in the liver, which were attenuated by rosiglitazone. Hepatic peroxisomal fatty acid β-oxidation was suppressed by ethanol in associated with inhibition of acyl-coenzyme A oxidase 1. Rosiglitazone elevated plasma adiponectin level and normalized peroxisomal fatty acid β-oxidation rate. However, rosiglitazone did not affect ethanol-reduced very low-density lipoprotein secretion from the liver. These results demonstrated that activation of PPAR-γ by rosiglitazone reverses ethanol-induced adipose dysfunction and lipid dyshomeostasis at the WAT-liver axis, thereby abrogating alcoholic fatty liver.
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